Overview: Cells sharing the same genome can exist in different phenotypes, raising a long-standing fundamental question in developmental biology: how a fertilized egg differentiates into cell types with distinct physical, chemical, and biological properties? Recent Nobel prize-winning work on cell reprogramming further indicates the importance of understanding how a cell controls its phenotype by regulating its gene expression program. Accumulating evidences reveal the critical role of epigenetic modifications on gene regulation. Epigenetic regulation refers to inheritable changes of gene expression caused not by changes in DNA sequence (i.e., mutations), but by non-genetic marks on chromatin (i.e., “epigenetic markers” such as DNA methylation and histone acetylation and methylation). Despite extensive studies, the quantitative nature of epigenetic regulation remains largely elusive.

The proposed research will use integrated experimental and computational approaches to reveal how histone modfications and gene transcription are coupled in mamallian cells.

Dr. Armaghan (Rumi) Naik and Dr. Joseph C. Ayoob received an award from the Mentoring in Active Learning and Teaching (MALT) Fellowship.

Naik, a Lane Fellow, aims to improve his teaching skills to better prepare himself for a tenure-track faculty position. He will do this work, under the direction of Joseph C. Ayoob, in the Laboratory Methods for Computational Biologists course.

“Understanding how genes co-evolve in animals could reveal links between human diseases”

Nathan Clark and his lab are looking at connections between what we think of as different diseases and how these connections can help lead to innovations in treatment of those diseases.

“By analyzing present-day genomic sequences through their relations to one another—in 33 different mammals, from elephants to platypuses to humans—Clark can infer the historical picture and pinpoint areas where genes show signs of rapid evolution. The degree to which these hot spots match across the animal kingdom is measured using something called ERC, or the “evolutionary rate covariation.”

For instance, if genes related to a particular function, say, color vision, are evolving at a similar rate between two species, then their ERC score would be quite high. Likewise, a high ERC score across a collection of related animals implies that they are all responding to a similar evolutionary pressure.

It may seem counterintuitive that species that are seemingly so different from us might provide insight into human diseases, but it is easy to forget how similar we are on the molecular level. “The genes that form a retina in a mouse are the same as the ones that form a retina in a kangaroo,” reminds Clark. And by evaluating the co-evolutionary signatures of genes related to these areas, we might be able to zero in on the individual genes or groups of genes that contribute to, say, retinal disease.

The University of Pittsburgh Cancer Institute and Pitt’s schools of medicine and graduate school of public health have received a five-year, $18 million federal grant to continue work on drugs that could provide protection during radiation emergencies, including acts of terrorism and reactor malfunctions.

This is the third time the grant from the National Institute of Allergy and Infectious Diseases has been renewed for Dr. Joel Greenberger, professor and chair of the Department of Radiation Oncology and his research team. It is one of only four awarded by NIAID.